Inflammation is an acknowledged component of age-associated conditions including frailty, hypertension, cardiovascular disorders, metabolic and neurodegenerative disorders such as Parkinsons and Alzheimers diseases. However, a key feature of age-associated inflammation is lack of significant overt manifestation of symptoms with increase in cytokines such as IL-1, IL-6 and TNF in the human blood that correlate with poor outcomes of several chronic age-related ailments. Other immunological features associated with chronic systemic inflammation include paucity and poor functional capability of lymphocytes. These changes are collectively referred to as inflammaging. Aging humans also experience gut-dysbiosis due to shortened telomeres, which create gut wall disintegration as well as a consequence of dietary insults to the gut lining. The goal of this project is to mimic age-associated low-grade inflammation in humans in young mice. We postulated that age-dependent impairment of gut integrity may permit low-level transfer of commensal bacteria or bacterial products to escape into the body, which would trigger variety of cell types to produce inflammatory agents that constitute low-grade systemic inflammation. Using this model we have shown that manifestation of PD is accelerated in A53T mouse model of PD.